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James Byrnes, C. Duval, Yiming Wang, Caroline Hansen, Byungwook Ahn, M. Mooberry, M. Clark, J. Johnsen, S. Lord, W. Lam, J. Meijers, H. Ni, R. Ariëns, A. Wolberg (2015)
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Arteriosclerosis, Thrombosis, and Vascular Biology RESEARCH LETTER VWF (von Willebrand Factor) Is Not Required for Red Blood Cell Retention in Clots in Mice Lori A. Holle , Dougald M. Monroe , Alisa S. Wolberg enous thrombosis and pulmonary embolism (collec- To investigate the contribution of VWF to RBC reten- tively venous thromboembolism) affect 1 to 2/1000 tion in clots, we collected blood from 18 to 22 week Vpeople annually. Venous thromboembolism has old wild-type (4 male, 3 female) or VWF-deficient ≈30% mortality, usually associated with pulmonary (B6.129S2-Vwf [tm1Wgr], 9 male, 4 female) C57BL6/J embolism and is the third leading cause of cardiovascu- mice (The Jackson Laboratory, Bar Harbor, ME) via infe- rior vena cava puncture into 3.2% sodium citrate (10% lar death worldwide. v/v, final). Data from males and females were not differ- Venous thrombosis is initiated by blood stasis and ent and were pooled for each genotype. Hematocrit was activation of coagulation, resulting in intravascular throm- similar between groups (39.2±1.1 versus 40.4±1.7%, bin generation and fibrin deposition. Trapping of red VWF-sufficient versus -deficient blood, respectively). We blood cells (RBCs) within the fibrin network and platelet- recalcified blood and triggered clotting with tissue factor mediated contraction of the thrombus
Arteriosclerosis, Thrombosis & Vascular Biology – Wolters Kluwer Health
Published: Aug 25, 2020
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